Journal of hypertension
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Journal of hypertension · Oct 1987
Pretreatment with vasodilator or V1-antagonist abolishes vasopressin withdrawal hypotension in spontaneously hypertensive rats.
In spontaneously hypertensive rats (SHR), the cessation of a 3-h intravenous infusion of arginine vasopressin (AVP, 8 mU/kg per min) resulted in a large and prolonged fall in arterial pressure (46 +/- 7.5 mmHg below basal levels). Pretreatment of SHR with the specific V1-receptor antagonist, [1-(beta-mercapto-beta, beta-cyclopentamethylene propionic acid), 2-(O-methyl)-tyrosine] AVP (d(CH2)5Tyr (Me)AVP, 8 micrograms/kg followed by 0.05 micrograms/kg per min) abolished the pressor response to AVP, and markedly reduced the subsequent hypotensive response following the cessation of the AVP infusion. ⋯ Finally, the concurrent administration of sodium nitroprusside (30 micrograms/kg per min) not only counteracted the pressure rise during AVP infusion, but also prevented the hypotensive response that normally accompanied the withdrawal of AVP. These findings demonstrate that neither V1-receptor activation nor blood pressure elevation alone was sufficient to generate a hypotensive response to the withdrawal of AVP; rather, both V1-receptor activation and a blood pressure elevation associated with the activation of these receptors were essential to the hypotensive response that followed the withdrawal of AVP in SHR.
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Recently, there has been an explosion of knowledge on vasopressin, including its neuro-anatomy, biochemistry and physiology. Recent work demonstrates extensive extra-hypothalamic vasopressinergic projections from the SON and PVN. Of particular importance are projections to the cardiovascular medullary centres. ⋯ Indeed, its volume retaining properties have probably been underestimated. Whereas in acute situations the vasoconstrictor properties may be of some importance, it is difficult to sustain long-term hypertension without maintenance of an adequate plasma volume. Vasopressin's central actions on the cardiovascular medullary centres, the baroreflex, the autonomic nervous system and catecholamine metabolism may also be involved in some hypertensive processes.(ABSTRACT TRUNCATED AT 400 WORDS)
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Journal of hypertension · Oct 1985
Comparative StudyHypotensive efficacy of a mixed solution of 0.1% sodium nitroprusside and 1% sodium thiosulphate.
A mixed solution of 0.1% sodium nitroprusside and 1% sodium thiosulphate ('SNP-thiosulphate') was given as i.v. infusion to 80 patients, 30 of whom were hypertensive emergencies and 50 were surgical cases requiring induction of hypotension. This treatment lowered the blood pressure (BP) by an average of 30% of the initial levels in the hypertensive patients and 30-40% of the initial levels in the surgical patients. The mean effective dose in the hypertensive patients was 2.4 micrograms/kg/min compared with about 3 micrograms/kg/min in 40 cases treated with sodium nitroprusside as mono-infusion. ⋯ In contrast to conventional therapy with SNP, the infusion of SNP-thiosulphate even at extremely high dose rates did not produce toxic concentrations of prussic acid in the blood. In no case was a rise observed in the cellular enzymes as an indirect indication of hypoxic cell damage. SNP-thiosulphate is thus at least as effective at lowering BP as SNP infused alone, and has a substantially lower toxicity risk.
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Journal of hypertension · Jun 1984
Comparative StudyCalf muscle haemodynamics and the renin-angiotensin-aldosterone system in normotensive subjects with a familial predisposition to hypertension: changes during increased salt intake.
Blood pressure, plethysmographically determined muscle blood flow in the calf at rest and during maximal dilatation, plasma renin activity, angiotensin II and plasma and urinary aldosterone were determined in normotensive men with a positive family history of hypertension (n = 17) and in an age- and weight-matched control group (n = 15) during usual sodium intake and after four weeks of increased salt intake. On normal salt intake resting muscle blood flow was significantly lower and resting resistance and resting vascular tone significantly higher in those with a positive family history, reflecting a stronger smooth muscle contraction of the resistance vessels in the calf at rest. Flow and resistance at maximal dilatation did not differ between the groups, indicating no difference in the structural design of the resistance vessels in the calf. ⋯ After four weeks of increased salt intake no significant changes were noted in blood pressure, muscle blood flow and resistance at rest or at maximal dilatation in either of the two groups. Plasma renin activity and angiotensin II decreased significantly in both groups after 10 days of increased salt but tended to return to normal values at the end of the fourth week. Plasma aldosterone and urinary aldosterone excretion were equally and significantly decreased in both groups giving no evidence for an inadequate suppression of aldosterone in subjects genetically predisposed to hypertension.